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 Table of Contents  
ORIGINAL ARTICLE
Year : 2019  |  Volume : 32  |  Issue : 3  |  Page : 932-937

Dialysis vintage and risk factors of hyperparathyroidism in hemodialysis patients


1 Department of Internal Medicine, Faculty of Medicine, Menoufia University, Menoufia, Egypt
2 Department of Nephrology, Health Insurance Sector, Tanta, Gharbia Governorate, Egypt

Date of Submission14-Nov-2017
Date of Acceptance20-Dec-2017
Date of Web Publication17-Oct-2019

Correspondence Address:
Mahmoud A Elsayed
Department of Nephrology, Health Insurance Sector, Tanta, Gharbia Governorate
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/mmj.mmj_797_17

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  Abstract 

Objective
The objective of this study was to study the risk factors of hyperparathyroidism based on hemodialysis vintage (duration in months or years that hemodialysis patients spend on dialysis).
Background
Hyperparathyroidism is associated with high risk of fractures, cardiovascular morbidity, and death; therefore, it is important to identify risk factors predicting or influencing parathyroid gland secretion.
Patients and methods
Patients were divided into two groups: short dialysis vintage (<10 years), and long dialysis vintage (≥10 years). Each group was further divided at parathyroid hormone (PTH) cutoff value of 300 pg/ml.
Results
Short dialysis vintage patients with PTH more than 300 pg/ml have higher alkaline phosphatase (147.9 ± 101.4 vs. 102.1 ± 89.18; P = 0.009), phosphorus (5.913 ± 1.621 vs. 5.044 ± 1.387; P = 0.048), calcium phosphate product (49.60 ± 13.45 vs. 42.35 ± 13.61; P = 0.04), and serum creatinine (10.8 ± 3.353 vs. 8.96 ± 2.311; P = 0.005 for predialysis serum creatinine and 4.987 ± 1.364 vs. 4.035 ± 1.426; P = 0.007 for postdialysis serum creatinine) compared with nonhigh PTH group. Long dialysis vintage patients with PTH more than 300 pg/ml have higher alkaline phosphatase (222.1 ± 184.7 vs. 99 ± 29.47; P = 0.024), lower serum sodium (137.3 ± 2.8 vs. 141.4 ± 2.937; P = 0.004), and lower mean arterial blood pressure (81.42 ± 14.65 vs. 96.38 ± 12.87; P = 0.019) compared with nonhigh PTH group.
Conclusion
Serum alkaline phosphatase, phosphorus, calcium phosphate product, and serum creatinine were found to be associated with hyperparathyroidism in short hemodialysis vintage patients (<10 years), but this association was lost in long dialysis vintage patients (≥10 years) except for 'alkaline phosphatase'. Moreover, serum sodium was found to be associated with hyperparathyroidism in long dialysis vintage patients.

Keywords: hemodialysis, hyperparathyroidism, vintage


How to cite this article:
Al Arbagy AR, Yassein YS, Emara MM, Elsayed MA. Dialysis vintage and risk factors of hyperparathyroidism in hemodialysis patients. Menoufia Med J 2019;32:932-7

How to cite this URL:
Al Arbagy AR, Yassein YS, Emara MM, Elsayed MA. Dialysis vintage and risk factors of hyperparathyroidism in hemodialysis patients. Menoufia Med J [serial online] 2019 [cited 2019 Nov 12];32:932-7. Available from: http://www.mmj.eg.net/text.asp?2019/32/3/932/268848




  Introduction Top


Secondary hyperparathyroidism is a major feature of chronic kidney disease (CKD) – mineral and bone disorder. Secondary hyperparathyroidism occurs in response to a series of abnormalities that initiate and maintain increased parathyroid hormone (PTH) secretion [1]. Uncontrolled hyperphosphatemia, hypocalcemia, and decreased synthesis of active vitamin D3 are three independent factors stimulating the secretion of PTH, leading to high turnover bone disease (osteitis fibrosa cystica) with increased osteoblastic and osteoclastic activity and bone marrow fibrosis with increased risk of fractures [1],[2]. Althoughfractures are associated with morbidity, mortality, and economic costs, there is a shortage of data regarding how to evaluate risk for fractures in CKD and how to treat high-risk patients [3]. Hyperparathyroidism is also associated with an increased risk of cardiovascular morbidity and death [4],[5], Hyperparathyroidism has been implicated in the pathogenesis of vascular calcification and hypertension in patients with CKD with increased risk of cardiovascular disease events [6] Other causes of hyperparathyroidism include increased fibroblast growth factor 23 concentration and the reduced expression of vitamin D receptors (VDRs), calcium-sensing receptors, fibroblast growth factor receptors, and klotho in the parathyroid glands [7],[8]. The aim was to study the risk factors of hyperparathyroidism in hemodialysis patients based on hemodialysis vintage (length of time in months or years that patients with end-stage renal disease spend on dialysis).


  Patients and Methods Top


The current study was carried out after obtaining a written consent from all patients and an approval by the Faculty of Medicine, Menoufia University Research Ethics Committee. The study started from June 2016 to May 2017. Inclusion criteria were patients on regular hemodialysis, age 18 years or older, hemodialysis for at least 3-month duration, mental competence, and willingness to participate in the study. Exclusion criteria included patients who had parathyroidectomy and/or receiving cinacalcet. The study was carried out at two dialysis centers belonging to Health Insurance Sector in Gharbia Governorate, Egypt (Almogamaa Eltibi Hospital Dialysis Center and El Mebara Hospital Dialysis Center). The number of patients who were on hemodialysis at mentioned dialysis centers at beginning of the study was 103. After excluding patients who had previous parathyroidectomy (eight patients), patients receiving cinacalcet treatment (two patients), one patient with dialysis dementia, and patients who were on regular dialysis for less than 3 months (two patients), 90 patients met our inclusion criteria and were included in our study. To study the influence of hemodialysis vintage on risk factors of hyperparathyroidism, at a vintage cutoff value of 10 years, all patients (90 patients) were divided into two groups: group I short dialysis vintage with vintage younger than 10 years (66 patients) and group II long dialysis vintage with vintage older than 10 years or more (24 patients). Each group was further divided at a PTH cutoff value of 300 pg/ml into two subgroups: group I into group Ia (23 patients), short dialysis vintage (dialysis duration <10 years) with intact parathyroid hormone (iPTH) more than 300 pg/ml, and group Ib (43 patients), short dialysis vintage (dialysis duration <10 years) with iPTH less than or equal to 300 pg/ml, whereas group II into group IIa (12 patients), long dialysis vintage (dialysis duration ≥10 years) with iPTH more than 300 pg/ml, and group IIb (12 patients), long dialysis vintage (dialysis duration ≥10 years) with iPTH less than or equal to 300 pg/ml. iPTH assay was done using electrochemiluminescence immunoassay by immunoanalyzer cobas E411 (Roche Diagnostics, Sandhofer Street, Mannheim, Germany) with iPTH reference range 15–65 pg/ml. 25 Hydroxyvitamin D, serum sodium, potassium, total and ionized calcium, phosphorus, alkaline phosphatase, hemoglobin, serum albumin, hepatitis C virus (HCV) antibodies titer, and uric acid samples were taken before dialysis. Serum creatinine and urea were sampled twice, before and after dialysis. Demographic data included in the analysis were age, sex, dry weight, BMI, blood pressure, medication history (daily elemental calcium dose and hemodialysis duration (vintage), history of chronic disease [diabetes mellitus (DM), hypertension (HTN), and ischemic heart disease (IHD)], and history of fractures. Calcium phosphate product was calculated by equation: [total calcium (mg/dl)×phosphorus (mg/dl)]. Urea reduction rate was calculated by equation [(urea predialysis − urea postdialysis)/urea predialysis].

Statistical analysis

The collected data were analyzed by statistical package of social science program (released 2011; IBM SPSS Statistics for Windows, version 20.0; IBM Corporation, Armonk, New York, USA). Qualitative data were expressed as number and percentage and analyzed by using χ2 and Fisher's exact tests. Quantitative data were expressed as mean ± SD and analyzed by using t-test and Mann–Whitney test.


  Results Top


A total of 90 patients were included in our study, including 57 (63.33%) males and 33 (36.66%) females. There were 35 patients with elevated PTH expression (PTH >300 pg/ml) and 55 patients with PTH less than or equal to 300 pg/ml. The comorbid conditions included HTN (62.2%), DM (16.6%), IHD (36.6%), adult polycystic kidney disease (10%), and systemic lupus erythematosus (2.2%); moreover, 66.6% of patients were positive for HCV antibodies. On comparison of mean values of patient's parameters according to PTH in patients with short dialysis vintage (66 patients), age distribution according to PTH has no significant difference between hyperparathyroidism group 'PTH more than 300 pg/ml' and nonhigh PTH group 'PTH less than or equal to 300 pg/ml' (53.26 ± 12.52 vs. 57.19 ± 9.04; P = 0.147) [Table 1], sex distribution had no significant difference between high and nonhigh PTH group (P = 0.459) [Table 1]. The comorbid conditions (DM, HTN, IHD, and HCV positivity) distribution according to PTH had no significant difference (P = 1.00, 0.220, 0.464, and 0.938, respectively) [Table 1]. Analysis of laboratory data showed that there is significant difference in the distribution of alkaline phosphatase between high and nonhigh PTH groups (147.9 ± 101.4 vs. 102.1 ± 89.18; P = 0.009). There is significant difference in the distribution of predialysis and postdialysis serum creatinine levels between high and nonhigh PTH group (10.8 ± 3.353 vs. 8.96 ± 2.311, P = 0.005, for predialysis serum creatinine and 4.987 ± 1.364 vs. 4.035 ± 1.426, P = 0.007, for postdialysis serum creatinine); patients with iPTH more than 300 pg/ml had higher levels of predialysis and postdialysis serum creatinine. Analysis of serum phosphorus showed that patients with iPTH more than 300 pg/ml had higher levels of serum phosphorus when compared to nonhigh PTH group 'PTH less than or equal to 300 pg/ml' (5.913 ± 1.621 vs. 5.044 ± 1.387; P = 0.048). There was a significant difference in the means of calcium phosphate product between high and nonhigh PTH group (49.60 ± 13.45 vs. 42.35 ± 13.61; P = 0.04) [Table 2]. There was no significant difference in the distribution of other parameters tested according to PTH in short vintage patients. On comparison of mean values of patient's parameters according to PTH in patients with long dialysis vintage (24 patients), age distribution according to PTH has no significant difference between high 'PTH more than 300 pg/ml' and nonhigh PTH group 'PTH less than or equal to 300 pg/ml' (52.171 ± 12.66 vs. 53.58 ± 10.6; P = 0.862) and sex distribution had no significant difference between high and nonhigh PTH group (P = 0.640) [Table 3]. The comorbid conditions (DM, HTN, IHD, HCV positivity) distribution according to PTH had no significant difference [Table 3]. There was a significant difference in the distribution of alkaline phosphatase between high and nonhigh PTH groups (222.1 ± 184.7 vs. 99 ± 29.47; P = 0.024). Analysis of serum sodium showed significant difference in the distribution of serum sodium between hyperparathyroidism group (PTH >300 pg/ml) and nonhigh PTH group (PTH ≤300 pg/ml); long dialysis vintage patients with hyperparathyroidism had lower levels of serum sodium compared with patients with iPTH less than or equal to 300 pg/ml (137.3 ± 2.8 vs. 141.4 ± 2.937; P = 0.004). Analysis of clinical data showed that long dialysis vintage patients with hyperparathyroidism had relatively lower mean arterial blood pressure levels when compared with long vintage patients with PTH less than or equal to 300 pg/ml (81.42 ± 14.65 vs. 96.38 ± 12.87; P = 0.019) [Table 4]. There was no significant difference in the distribution of other parameters tested according to PTH in long vintage patients.
Table 1: Demographic data and clinical history of patients according to parathyroid hormone in patients with short dialysis vintage

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Table 2: Mean values of patient's parameters according to intact parathyroid hormone (more than and <300 pg/ml) in short dialysis vintage patients

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Table 3: Demographic data and clinical history of patients according to parathyroid hormone in patients with long dialysis vintage

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Table 4: Mean values of patient's parameters according to intact parathyroid hormone (more than and <300 pg/ml) in long dialysis vintage patients

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  Discussion Top


Many studies including ours have suggested strong correlation between serum PTH in hemodialysis patients and alkaline phosphatase. Saravani et al. [9] showed direct correlation between PTH and alkaline phosphatase; moreover, Blayney et al. [10] found that significantly elevated alkaline phosphatase values were predicted by higher PTH levels. Maruyama et al. [11] reviewed baseline data of 185 277 hemodialysis patients extracted from a nationwide dialysis registry at the end of 2009 in Japan and found that a higher alkaline phosphatase was also associated with higher iPTH levels, lower albumin, and higher C-reactive protein. Li et al. [12] investigated the association between serum iPTH level and the risk of high serum alkaline phosphatase and found that alkaline phosphatase was strictly correlated with serum iPTH range, which corresponds with the current study. Analysis of predialysis and postdialysis serum creatinine in short dialysis vintage patients showed significant difference in the distribution of predialysis and postdialysis serum creatinine between hyperparathyroidism group (PTH >300 pg/ml) and nonhigh PTH group (PTH ≤300 pg/ml); patients with iPTH more than 300 pg/ml had higher levels of predialysis and postdialysis serum creatinine compared with patients with iPTH less than or equal to 300 pg/ml. Serum creatinine expression levels are a commonly used index assessing the glomerular filtration rate. According to KDOQI guidelines, once the glomerular filtration rate is less than 60 ml/min, PTH expression levels increase. Wei et al. [8] found that PTH is negatively correlated with serum creatinine expression levels in patients with CKD. Avram et al. [13] stated that PTH level is correlated with serum creatinine in hemodialysis patients but only with serum creatinine before dialysis, with a conclusion that patients with higher PTH were better nourished than those with lower PTH.

Analysis of serum phosphorus and calcium phosphate product in short dialysis vintage patients showed that there is significant difference in the means of phosphorus and calcium phosphate product between hyperparathyroidism group (PTH >300 pg/ml) and nonhigh PTH group (PTH ≤300 pg/ml); patients with iPTH more than 300 pg/ml had higher levels of serum phosphorus and calcium phosphate product compared with the nonhigh PTH group. A systematic review of the literature of eight studies describing the distribution of renal osteodystrophy among patients with CKD on dialysis by Khan and Iraniha [14] showed that 221 patients had low turnover whereas 303 patients had high turnover bone disease. Mean values of phosphorus in the mentioned groups were 5.5 ± 3.28 (n = 221) and 6.12 ± 3.28 (n = 303), respectively. There was a significant difference between the two groups (P = 0.03), which means that the high turnover state of hyperparathyroidism is closely correlated with higher levels of phosphorus, which corresponds with the present study. Adhikary et al. [15] found that calcium phosphate product is closely associated with raised level of serum iPTH and stated that the relation may guide physician to suspect hyperparathyroidism in patients with CKD. Sliem et al. [16] showed that PTH has a significant positive correlation with serum phosphorus level. Moreover, Fine et al. [17] found that elevation of serum phosphate affects PTH levels in 50% of hemodialysis patients, which is unrelated to changes in serum calcium. Effect of phosphorus on increasing iPTH secretion was illustrated in many studies like Finch et al. [18], Ho et al. [19], and Slatopolsky et al. [20]. Analysis of serum sodium in long dialysis vintage patients showed significant difference in the distribution of serum sodium between hyperparathyroidism group (group IIa) and nonhigh PTH group (group IIb); long dialysis vintage patients with hyperparathyroidism (PTH >300 pg/ml) had lower levels of serum sodium compared to nonhigh PTH group with PTH less than or equal to 300 pg/ml [Table 4]. Smith et al. [21] studied the effect of both exogenous and endogenous PTH on sodium and found that both exogenous and endogenous PTH levels can elevate plasma renin activity and increase sodium excretion through the kidney, causing relative hyponatremia; however, this mechanism does not explain the negative correlation between iPTH and serum sodium in our study, as this patient group (group IIa) was already on hemodialysis for more than 10 years with almost no residual renal function. Tordoff [22] in an experimental study on rats found that sodium chloride ingestion leads to elevated plasma ionized calcium and reduced PTH; however, the mechanism is unknown. Although, Drüeke et al. [23] studied the direct effect of PTH on intestinal sodium absorption and stated that PTH has a direct inhibitory effect on jejunal sodium absorption.

Analysis of clinical data showed that long dialysis vintage patients with hyperparathyroidism (PTH >300 pg/ml) (group IIa) had relatively lower mean arterial blood pressure levels when compared with patients with PTH less than or equal to 300 pg/ml (group IIb) [Table 4]. PTH directly stimulates the renin angiotensin–aldosterone system and the sympathetic nervous system, resulting in increases in arterial blood pressure [24],[25]. However, this association is reversed in long dialysis vintage patients in the current study. We assume this to the relatively lower concentrations of sodium in this group (group IIa) 'hyperparathyroidism patients with long dialysis vintage group', as there is a positive association between serum sodium levels and blood pressure in hemodialysis patients [26]. There was no significant difference in the distribution of phosphorus, calcium phosphate product, and serum creatinine according to PTH in long dialysis vintage patients group (group II). The nature of renal osteodystrophy may differ between the early and late stages of CKD with less response at the later stages to external influences. Parathyroid cell proliferation is initially polyclonal, but later on it may be complicated by monoclonal or multiclonal proliferation, which is a characteristic of severe and autonomous forms of hyperparathyroidism [27]. Most parathyroid glands removed surgically from patients with uremia with severe forms of secondary hyperparathyroidism are nodular, with a reduction in VDR and calcium-sensing receptor expression, indicating a reduced capacity to respond to therapy [28]. Difference in parathyroid cell proliferation together with reduction of VDR and calcium receptor expression may explain why correlation of iPTH to phosphorus, calcium phosphate product, and serum creatinine was lost in patients with long dialysis vintage in the current study.


  Conclusion Top


Serum alkaline phosphatase, phosphorus, calcium phosphate product, and serum creatinine were found to be associated with hyperparathyroidism in short hemodialysis vintage patients (<10 years), but this association was lost in long dialysis vintage patients (≥10 years) except for 'alkaline phosphatase'. Moreover, serum sodium was found to be associated with hyperparathyroidism in long dialysis vintage patients.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
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    Tables

  [Table 1], [Table 2], [Table 3], [Table 4]



 

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